A5051120536- Liver Disease Diagnosis and Treatment
- Alcohol Consumption and Health Effects
- Hepatitis C virus research
- Hepatitis B Virus Studies
- Endoplasmic Reticulum Stress and Disease
- Ubiquitin and proteasome pathways
- Diet, Metabolism, and Disease
- Lipid metabolism and biosynthesis
- Phagocytosis and Immune Regulation
- HIV Research and Treatment
- Peroxisome Proliferator-Activated Receptors
- Liver physiology and pathology
- Folate and B Vitamins Research
- Pancreatic function and diabetes
- HIV-related health complications and treatments
- Immune Cell Function and Interaction
- Adipose Tissue and Metabolism
- Drug-Induced Hepatotoxicity and Protection
- Mast cells and histamine
- Liver Disease and Transplantation
- Immune Response and Inflammation
- Autophagy in Disease and Therapy
- Diabetes and associated disorders
- Muscle metabolism and nutrition
- Cytokine Signaling Pathways and Interactions
University of Nebraska Medical Center
2016-2025
VA Nebraska Western Iowa Health Care System
2014-2023
University of Nebraska at Omaha
2005-2022
Nebraska Medical Center
2016-2020
Omaha VA Medical Center
2004-2019
University of Nottingham
2016
Royal Derby Hospital
2016
University of Louisville
2016
University of Colorado Denver
2016
Cedars-Sinai Medical Center
2016
Primary nonalcoholic fatty liver disease (NAFLD) is bi-directionally associated with the metabolic syndrome and its constitutive features ("factors": impaired glucose disposal, visceral obesity, arterial hypertension, dyslipidemia). Secondary NAFLD occurs due to endocrinologic disturbances or other cofactors. This nosography tends be outdated by novel definition of (MAFLD). Irrespective nomenclature, this condition exhibits a remarkable pathogenic heterogeneity unpredictable clinical...
Introduction . Mitochondrial damage and disruption in oxidative phosphorylation contributes to the pathogenesis of alcoholic liver injury. Herein, we tested hypothesis that hepatoprotective actions betaine against injury occur at level mitochondrial proteome. Methods Male Wister rats were pair-fed control or ethanol-containing liquid diets supplemented with without (10 mg/mL) for 4-5 wks. Liver was examined triglyceride accumulation, levels methionine cycle metabolites, alterations proteins....
Human-specific HIV-1 and hepatitis co-infections significantly affect patient management call for new therapeutic options. Small xenotransplantation models with human hepatocytes hematolymphoid tissue should facilitate antiviral/antiretroviral drug trials. However, experience mouse strains tested dual reconstitution is limited, technical difficulties such as risky manipulations newborns high mortality rates due to metabolic abnormalities. The best animal hepatocyte transplantation are not...
Binge drinking is the most common form of excessive alcohol use. Repeated episodes binge cause multiple organ injuries, including liver damage. We previously demonstrated that chronic ethanol administration causes a decline in intrahepatic ratio S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH). This impairments essential methylation reactions result alcohol-induced fatty (steatosis) and other features alcohol-associated disease (ALD). Co-treatment with betaine during feeding,...
About 296 million people worldwide are living with chronic hepatitis B viral (HBV) infection, and outcomes to end-stage liver diseases potentiated by alcohol. HBV replicates in hepatocytes, but other non-parenchymal cells can sense the virus. In this study, we aimed investigate regulatory effects of macrophages on marker interferon-stimulated genes (ISGs) expressions hepatocytes. This study was performed HBV-replicating HepG2.2.15 human monocyte-derived (MDMs). We found that exposure an...
Alcohol consumption exacerbates the pathogenesis of hepatitis C virus (HCV) infection and worsens disease outcomes. The exact reasons are not clear yet, but they might be partially attributed to ability alcohol further suppress innate immunity. Innate immunity is known already decreased by HCV in liver cells.In this study, we aimed explore mechanisms how metabolism dysregulates IFNα signaling (STAT1 phosphorylation) HCV+ hepatoma cells. To end, CYP2E1+ Huh7.5 cells were infected with exposed...
Alcohol exposure worsens the course and outcomes of hepatitis C virus (HCV) infection. Activation protective antiviral genes is induced by IFN-α signaling, which altered in liver cells either HCV or ethanol exposure. However, mechanisms combined effects metabolism signaling modulation are not well elucidated. Here, we explored a possibility that potentiates HCV-mediated dysregulation via impairment methylation reactions. HCV-infected Huh7.5 CYP2E1(+) human hepatocytes were exposed to...